Under the nutritional pressure of lack of glucose or glutamine, tumor cells activate the oncogene c-Myc, metabolize enzyme expression by regulating the serine synthesis pathway molecules such as PHGDH, PSAT1, and PSPH, use the remaining glutamine or glucose to support the de novo serine synthesis pathway, and support tumor cell survival under nutritional stress by maintaining redox homeostasis (27). The gene discussed is MYC; the disease is neoplasm.